INTRACELLULAR OXYGEN-TENSION AND ENERGY-METABOLISM IN THE CAT BRAIN CORTEX DURING HEMORRHAGIC-SHOCK

  • 1 January 1979
    • journal article
    • research article
    • Vol. 54  (4) , 333-346
Abstract
The changes in intracellular O2 tension and energy metabolism of the cat brain cortex were studied by surface fluororeflectometry during hemorrhagic shock. Intracellular O2 tension, i.e., the maximum cortical NAD reduction obtained during N gas inhalation decreased gradually during the hypovolemic phase of shock and finally, the brain cortex became ischemic. Partial uncoupling of the cerebrocortical mitochondrial respiration and oxidative phosphorylation appeared in the very early period of bleeding, as indicated by the overshot of the cortical NAD/NADH redox state towards oxidation subsequent to the cessation of N gas inhalation. Partial uncoupling of mitochondrial respiration and oxidative phosphorylation became more pronounced during the later phases of bleeding, finally, the mitochondrial electron transport stopped. In line with these changes the frequency and the amplitude of ECoG (electrocorticogram) decreased gradually and markedly during the hypovolemic phase of shock. Microcirculation and energy metabolism of the cat brain cortex were severely and irreversibly damaged during the hypovolemic phase of shock. In the majority of experiments the N anoxia after reinfusion failed to bring about changes in the cortical NAD/NADH redox state and the ECoG changes occurring during bleeding did not improve after reinfusion. The early disturbances of cerebrocortical energy metabolism play an important role in the development of neural and vascular lesions of the brain that occur during hemorrhagic shock.